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Fay, Mike; Longo, Kenneth A.; Karathanasis, George A; Shope, David M; Mandernach, Craig J; Leong, Jason; Hicks, Alfred; Pherson, Kenneth; Husain, Amyna

doi:10.1186/1476-4598-2-40

Cited by 50 publications

(22 citation statements)

References 71 publications

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“…An increase in Cul5 expression with granulocytic differentiation is not totally unexpected, as overexpression of Cul5 inhibits proliferation in CHO, COS-1, and T47D cell lines (Van Dort et al 2003;Burnatowska-Hledin et al 2004), and Cul5 plays a role in cell fate determination in Drosophila (Ayyub et al 2005). Additional studies also support a putative tumor suppressor role for Cul5 in breast cancer, as the chromosomal location (11q22-23) for Cul5 is associated with loss of heterozygosity (Carter et al 1994;Hampton et al 1994;Gudmundsson et al 1995;Negrini et al 1995;Tomlinson et al 1995;Winqvist et al 1995;Byrd et al 1997;Driouch et al 1998) and there is decreased expression of Cul5 in breast tumor tissues versus matched normal tissues (Fay et al 2003). A 1.6-fold change in Cul5 mRNA expression, and a 6.5-fold change in Cul5 protein expression, may have an important role in cellular processes such as differentiation since a previous study indicated that a less than twofold increase in the expression of another cullin family member, Cul4A, promotes proliferation and attenuates granulocytic differentiation of the PLB-985 human myeloid leukemia cell line .…”

Section: Discussionmentioning

confidence: 87%

“…Cellular protein was isolated using the M-PER® (Pierce, Rockford, IL) mammalian protein extraction reagent supplemented with a complete™ mini protease inhibitor cocktail tablet (Roche Molecular Biochemicals, Indianapolis, IN) as previously described (Fay et al 2003). To facilitate equal loading between samples, protein concentrations were determined using the BCA™ kit (Pierce).…”

Section: Methodsmentioning

confidence: 99%

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Granulocytic differentiation of HL-60 promyelocytic leukemia cells is associated with increased expression of Cul5

Baxter

Carlson

Mayer

et al. 2009

In Vitro Cell.Dev.Biol.-Animal

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The human HL-60 promyelocytic leukemia cell line has been widely used as a model for studying granulocytic differentiation. All-trans retinoic acid (ATRA) treatment of HL-60 cells promotes granulocytic differentiation and is effective as differentiation therapy for patients with acute promyelocytic leukemia. The identification of genes that are transcriptionally regulated by ATRA has provided insight into granulocytic differentiation and differentiation therapy. The Asb-2 (ankyrin repeat SOCS box 2) gene has previously been identified as a transcriptional target in ATRA-treated HL-60 cells. The ASB-2 protein forms an E3 ubiquitin ligase complex with the proteins, Cul5, regulator of cullin 2 (ROC2), and elongin B and C. The purpose of this study was to determine if there is increased expression of Cul5 during granulocytic differentiation of HL-60 cells. To induce granulocytic differentiation, HL-60 cells were treated for 5 d with ATRA and differentiation was confirmed by examining superoxide anion production, nuclear morphology, and changes in the expression of CD11b, CD13, and CD15. Quantitative real-time RT-PCR was used to measure Cul5 mRNA expression and also the expression of other components of the E3 ubiquitin ligase (ASB-2, ROC2, elongin B and C). Granulocytic differentiation of HL-60 cells was associated with a 1.6-, 1.7-, and 23-fold statistically significant (P

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Section: Discussionmentioning

confidence: 87%

Section: Methodsmentioning

confidence: 99%

Granulocytic differentiation of HL-60 promyelocytic leukemia cells is associated with increased expression of Cul5

Baxter

Carlson

Mayer

et al. 2009

In Vitro Cell.Dev.Biol.-Animal

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“…NLK and DEDD are suggested to induce apoptosis [31, 32] and loss of RAB1B was shown to enhance the aggressiveness of breast carcinoma [33]. A reduction of CUL5 expression was found, for instance, in breast cancer [34], but so far not in prostate carcinoma. Finally, PRDX3 was chosen as it was previously found to be upregulated in primary PCa [35].…”

Section: Resultsmentioning

confidence: 99%

Analysis of Argonaute Complex Bound mRNAs in DU145 Prostate Carcinoma Cells Reveals New miRNA Target Genes

Szczyrba

Jung

Beitzinger³

et al. 2017

Prostate Cancer

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Posttranscriptional gene regulation by microRNAs (miRNAs) contributes to the induction and maintenance of prostate carcinoma (PCa). To identify mRNAs enriched or removed from Ago2-containing RISC complexes, these complexes were immunoprecipitated from normal prostate fibroblasts (PNFs) and the PCa line DU145 and the bound mRNAs were quantified by microarray. The analysis of Ago complexes derived from PNFs or DU145 confirmed the enrichment or depletion of a variety of mRNAs already known from the literature to be deregulated. Novel potential targets were analyzed by luciferase assays with miRNAs known to be deregulated in PCa. We demonstrate that the mRNAs of the death effector domain-containing protein (DEDD), the tumor necrosis factor receptor superfamily, member 10b protein (TNFRSF10B), the tumor protein p53 inducible nuclear protein 1 (TP53INP1), and the secreted protein, acidic, cysteine-rich (SPARC; osteonectin) are regulated by miRNAs miR-148a, miR-20a, miR-24, and miR-29a/b, respectively. Therefore, these miRNAs represent potential targets for therapy. Surprisingly, overexpression of miR-24 induced focus formation and proliferation of DU145 cells, while miR-29b reduced proliferation. The study confirms genes deregulated in PCa by virtue of their presence/absence in the Ago2-complex. In conjunction with the already published miRNA profiles of PCa, the data can be used to identify miRNA-regulated mRNAs.

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“…Most notably, COMMD1 and Cul5 expression was found to be decreased or lost in a number of human tumors [37], [38]. However, with respect to the expression pattern of these proteins upon Hsp90 inhibition, no differences were detectable in H1339 and EPLC-272H tumor cells.…”

Section: Discussionmentioning

confidence: 96%

Radiosensitization of Normoxic and Hypoxic H1339 Lung Tumor Cells by Heat Shock Protein 90 Inhibition Is Independent of Hypoxia Inducible Factor-1α

Schilling

Bayer

et al. 2012

PLoS ONE

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BackgroundIonizing irradiation is a commonly accepted treatment modality for lung cancer patients. However, the clinical outcome is hampered by normal tissue toxicity and tumor hypoxia. Since tumors often have higher levels of active heat shock protein 90 (Hsp90) than normal tissues, targeting of Hsp90 might provide a promising strategy to sensitize tumors towards irradiation. Hsp90 client proteins include oncogenic signaling proteins, cell cycle activators, growth factor receptors and hypoxia inducible factor-1α (HIF-1α). Overexpression of HIF-1α is assumed to promote malignant transformation and tumor progression and thus might reduce the accessibility to radiotherapy.Methodology/Principal FindingsHerein, we describe the effects of the novel Hsp90 inhibitor NVP-AUY922 and 17-allylamino-17-demethoxygeldanamycin (17-AAG), as a control, on HIF-1α levels and radiosensitivity of lung carcinoma cells under normoxic and hypoxic conditions. NVP-AUY922 exhibited a similar biological activity to that of 17-AAG, but at only 1/10 of the dose. As expected, both inhibitors reduced basal and hypoxia-induced HIF-1α levels in EPLC-272H lung carcinoma cells. However, despite a down-regulation of HIF-1α upon Hsp90 inhibition, sensitivity towards irradiation remained unaltered in EPLC-272H cells under normoxic and hypoxic conditions. In contrast, treatment of H1339 lung carcinoma cells with NVP-AUY922 and 17-AAG resulted in a significant up-regulation of their initially high HIF-1α levels and a concomitant increase in radiosensitivity.Conclusions/SignificanceIn summary, our data show a HIF-1α-independent radiosensitization of normoxic and hypoxic H1339 lung cancer cells by Hsp90 inhibition.

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Untitled

Cited by 50 publications

References 71 publications

Granulocytic differentiation of HL-60 promyelocytic leukemia cells is associated with increased expression of Cul5

Granulocytic differentiation of HL-60 promyelocytic leukemia cells is associated with increased expression of Cul5

Analysis of Argonaute Complex Bound mRNAs in DU145 Prostate Carcinoma Cells Reveals New miRNA Target Genes

Radiosensitization of Normoxic and Hypoxic H1339 Lung Tumor Cells by Heat Shock Protein 90 Inhibition Is Independent of Hypoxia Inducible Factor-1α

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